Incidence
Age
Sex
Geography
Aetiology	- presence of fluid in the peritoneal cavity Pathogenesis - sodium and water retention due to peripheral arterial vasodilatation -> reduction in effective arerial volume - NO, AVP and prostaglandins have been implicated - sympathetic NS and rnin-angiotensin system are activated in response to reduced effective volume -> water and salt retention - increased local hydrostatic pressure in the portal system leads to exudation of lymph and transudation of fluid into peritoneal cavity - low serum albumin due to poor hepatic synthesis ---> positive sodium balance of 90-170 mmol/day Causes of straw-coloured ascitic fluid - malignancy - cirrhosis - infective - TB, following bowel perforation, spontaneous infection in cirrhotics - hepatic vein obstruction (Budd-Chiari syndrome) - chronic pancreatitis - congestive cardiac failure - constrictive pericarditis - Meigs' syndrome (ovarian tumour) - hypoproteinaemia (e.g. nephrotic syndrome) Causes of chylous ascitic fluid - obstruction of main lymphatic duct by e.g. carcinoma Causes of haemorrhagic ascitic fluid - Malignancy - ruptured ectopic pregnancy - abdominal trauma - acute pancreatitis
Presentation	- abdominal swelling - may have fast or slow course - mild generalized abdominal pain/discomfort - tense ascites may produce respiratory distress - shifting dullness - may be pleural effusion (usually right-sided)
Investigations	Aspirate ascites - 10-20 ml diagnostic aspirate - cell count - neutrophils > 250 cells/mm3 indicates bacterial peritonitis - gram stain and culture (including AFBs) - protein - ascitic protein more than 11 g/L less than serum albumin level suggests a transudate - cytology - amylase (exclude pancreatic ascites) Bloods for serum albumin During treatment - U+Es, creatinine every other day - daily urinary outputs
Macro
Micro
Staging
Serum markers	- AFP
Management	- aim is to reduce sodium intake, increase renal soduim excretion ---> reabsorption of fluid from ascites into systemic circulation; the maximum rate for at which this occurs is 500-700 mL/24 hours Dietary restriction of sodium - ideally to 22 mmol/24 hours; however, a compromise of 40 mmol/24 hours is achieved more often Diuretics - spironolactone 200 mg od - causes gynaecomastia with chronic use; at this point amiloride 10-15 mg od is substituted - response is often poor; spironolactone 500 mg may be used - frusemide 80mg or bumetanide 1 mg daily may be used if patient fails to respond - ascitic fluid takes longer to mobilize than interstitial fluid - care should be taken when giving diuretics to patients without peripheral oedema; a rise in serum creatinine indicates overdiuresis ---> temporarily discontine diuretics - hyponatraemia indicates haemodilution secondary to a failure to clear free water; this is generally due to reduced renal perfusion - diuretics should also be stopped if there is hypokalaemia Paracentesis - used to relieve symptomatic tense ascites - unfortunately, the ascites tends to reaccumulate at the expense of circulating volume -> hypovolaemia - if the patient has normal renal function, albumin (6 g/L ascites removed) or plasma expanders can be used - should not be performed if the patient is in end-stage cirrhosis or has renal failure Shunts - peritoneo-venous shunt to internal jugular; useful in patients with resistent ascites, but tube often blocks - TIPS is occasionally helpful
Prognosis
Complications	Spontaneous bacterial peritonitis - occurs in 8% of cirrhotics with ascites - E. coli, Klebsiella and enterococci are the most common agents; thought to reach peritoneum via haematogenous spread - pain and pyrexia are frequently absent, but patient may deteriorate clinically - perform diagnostic aspiration - treat with 3rd gen cephalosporin, e.g. cefotaxime, ceftazidime - 50% mortality, recurs in 70% within a year - indicates transplant

Hepatobiliary medicine

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